脂肪细胞因子的负反馈作用与肥胖和2型糖尿病的形成

背景：通过分析脂肪细胞因子对机体的能量代谢及脂肪积累的调节作用，探讨脂肪组织的负反馈机制在肥胖、2型糖尿病形成中的作用。 资料来源：应用计算机检索美国国立医学图书馆PubMed数据库1962-01／2005—11有关脂肪细胞因子的负反馈作用，肥胖和2型糖尿病的文章，检索词为“adipocytokines，obesity，tumor necrosis factor-α，interleukin-6，leptin，adiponectin，msistin and PGAR”，限定语言种类为英语。 资料选择：选择原创性研究论文作为参考，同时限定论文的内容必须与机体的能量代谢及脂肪积累有关；去除重复性研究、综述和其他与机体的能量代谢及脂肪积累关系不大的资料。 资料提炼：共收集相关文献158篇，排除重复性研究和与本文主题相关性较小的文献123篇，本文共纳入文献35篇。 资料综合：最近的研究表明脂肪组织能够分泌脂肪细胞因子以调节自身的容量。当体脂增加，脂肪细胞因子的调节作用会抑制脂肪合成，增加脂肪分解。脂肪细胞因子主要是通过抵抗胰岛素作用和减少胰岛素分泌来抑制脂肪合成，使脂肪分解增加，游离脂肪酸水平升高，抑制了血糖的利用。 结论：当肥胖达到一定程度，脂肪细胞因子的负反馈作用可能是导致2型糖尿病发生的原因之一。     

脂联素水平与运动及机体肥胖的相关性

学术背景:脂联素在健康机体血浆中含量丰富,但在冠心病、肥胖、2型糖尿病及原发性高血压等疾病中,脂联素水平下降,且其下降程度与病情严重程度呈正相关.目的:分析近年来有关运动对肥胖与2型糖尿病患者机体脂联素水平的影响.检索策略:应用计算机检索PubMed数据库1995-01/2006-12有关脂联素与运动的文献.检索词“adiponectin,exercise“,限定文章语言种类为English.同时计算机检索中文数据库CNKI 1995-01/2006-12有关脂联素与运动的文献,检索词“脂联素,运动“,限定文章语言种类为中文.共收集到51篇相关文献.对资料进行初审,选取所有运动与脂联素水平相关的文献,并查找原文.纳入标准:重点选择有关探讨运动对肥胖及2型糖尿病患者脂联素影响的文献.排除标准:重复研究.文献评价:排除19篇因研究目的与本研究无关的文献,最终纳入符合标准的文献32篇.资料综合:脂联素是脂肪细胞特异分泌的一种激素蛋白,具有调节能量平衡、增强胰岛素敏感性、抗动脉粥样硬化及抗炎等广泛的生物学作用,是肥胖与糖尿病患者体内第一个下调的脂肪因子,与胰岛素抵抗的发生发展密切相关.运动作为一种对机体有益的刺激因子能否影响肥胖及糖尿病患者体内脂联素水平,或通过刺激内源性脂联素增加从而改善患者体内胰岛素抵抗,是近年来研究运动与脂联素的热点之一.文章在介绍脂联素生物学概况的基础上,对近年来有关运动对肥胖及糖尿病患者脂联素水平影响的研究进行了评述.结论:由于脂联素所具有的机体保护作用,近年来有关运动对肥胖及糖尿病患者脂联素水平影响的研究结果不够一致,仍需进一步的深入研究,尤其需要从机制方面进行探讨.     

脂肪组织与骨骼肌信号之间的分子代谢关系

学术背景:最近研究发现脂肪组织与骨骼肌之间有着某种联系。脂肪组织能分泌许多细胞因子,对体质量调节起着重要作用。然而骨骼肌在代谢调节方面可能与脂肪组织有相似的作用。目的:探讨骨骼肌与脂肪组织之间的关系,说明骨骼肌在控制体质量方面的作用。检索策略:应用计算机检索CMBI、NCBI据库1994-01/2005-12相关骨骼肌、脂肪组织、肥胖等方面的文献,检索词"Skeletal muscle,Adipose tissue",限定文献语言种类为English。对资料进行初审,选取包括骨骼肌、脂肪组织、瘦素与细胞因子的文献,开始查找全文。纳入标准:①具有原创性,论点论据可靠的实验文章。②观点明确,分析全面的文章。③文献主体内容与此课题联系紧密的文章。排除标准:实验设计不合理的文章及观点模糊的综述。文献评价:共检索到109篇关于骨骼肌、脂肪组织与细胞因子的文献,最终纳入47篇符合标准的文献。资料综合:脂肪组织在能量稳态中起重要作用,能分泌一些细胞因子。这些细胞因子的表达或活性的改变对肥胖和胰岛素抵抗等病理状态有着重要作用。然而骨骼肌在代谢调节方面可能与脂肪组织有相似的作用。有研究证明在骨骼肌中表达的一些细胞因子确实可以调节脂肪代谢。本文综述了脂肪组织和骨骼肌信号之间的代谢关系。这两种组织的细胞因子在维持脂肪组织和骨骼肌足够比率方面有重要作用,因而在体质量控制方面亦有重要作用。白细胞介素15(在骨骼肌中高度表达)、肿瘤坏死因子α和瘦素在脂肪组织与骨骼肌之间联系中起着重要作用。结论:脂肪组织与骨骼肌之间可能存在联系,而且与体质量控制有关,包括脂肪储存和肌肉质量的控制。     

运动减肥的生物学机制

目的:体育运动是一种可以用于减肥和预防肥胖并发症的有效途径,针对运动对肥胖的生物学作用,以及运动的科学性和肥胖的特殊性运动减肥,产生了许多相关的理论与实践。资料来源:应用计算机检索Sportdiscuss1999-01/2006-09与运动减肥相关的文章,检索词“exercise or sports,obesity”,并限定文章语言种类为“English”,文章来源限定为“Journals article”;同时计算机检索CNKI1999-01/2006-09的相关文章,检索词“运动、肥胖”,并限定语言种类为中文;同时手工查阅相关书籍。资料选择:对资料进行初审,文献纳入标准:①肥胖治疗的最新方法。②肥胖产生的机制。③运动对肥胖的作用。④运动减肥处方。排除重复性研究的文献。资料提炼:在CNKI中共检索到22篇相关文章,均检索全文,17篇符合纳入标准,排除2篇重复性研究和2篇无意义研究;在Sportdiscuss数据库中检索到相关文献39篇,符合要求者21篇;同时录入书籍3本。资料综合:①肥胖的产生原因:肥胖受遗传因素、营养因素、生理因素、代谢因素、行为因素、环境因素、社会因素、甚至种族因素的影响。②运动对肥胖的生物学作用:运动能增加能量消耗,调节能量平衡;减少体脂,改善身体成分组成;调节胰岛素代谢,改善脂代谢,还能调节肥胖基因的表达,在一定程度上抗衡基因的缺陷。③运动减肥处方:以有氧运动作为运动项目,增强耐力,提高心肺功能。每次运动时间应持续30～60min,中低强度,3～5次/周,最好1次/d。结论:有氧运动可通过改变体脂含量、调节能量代谢、脂代谢、胰岛素代谢以及肥胖基因的表达达到减肥的目的,长期坚持科学的有氧运动是目前较合理、有效的方法。     

中药及天然药物有效成分改善脂肪细胞胰岛素抵抗的机制

脂肪组织不仅是机体储存能量的主要场所,也是一个活跃的内分泌和旁分泌器官,可分泌多种脂肪细胞因子和激素。而脂肪过度堆积将伴随着胰岛素抵抗(IR)和2型糖尿病(T2DM)发病风险的增     

2型糖尿病发病机制研究:肿瘤坏死因子α与胰岛素抵抗的关系

目的:回顾肿瘤坏死因子α的生物学效应以及与胰岛素抵抗之间的关系,为糖尿病一级康复预防提供理论依据。资料来源:应用计算机检索ScienceDirect1996-01/2004-05期间的相关文章,检索词“tumornecrosisfactor-α,insulinresistance”,并限定文章语言种类为英文。同时计算机检索“中国期刊网”2003-01/2004-06期间的相关文章,限定文章语言种类为中文,检索词为“肿瘤坏死因子α,胰岛素抵抗”等。资料选择:对资料进行初审,选择肿瘤坏死因子α与胰岛素抵抗之间的相互作用的研究,治疗糖尿病的方法方面的实验研究。资料提炼:共收集到15篇关于肿瘤坏死因子α与胰岛素抵抗之间的作用以及减重与肥胖方面的文献。资料综合:肿瘤坏死因子α在肥胖动物模型及肥胖症患者的脂肪组织中过度表达,在与肥胖相关的胰岛素抵抗中起核心作用。实验研究也显示出减重治疗由肿瘤坏死因子α导致的糖尿病有一定疗效。结论:肿瘤坏死因子α与胰岛素抵抗之间分子水平联系的研究越来越细致化,糖尿病的治疗向分子水平及基因水平发展,为研究糖尿病发病机制,早期预防及运动干预和开发胰岛素抵抗药物奠定分子生物学基础。     

肥胖糖尿病患者腹内脂肪含量与脂肪细胞因子、胰岛素抵抗相关性研究

目的探讨肥胖2型糖尿病患者腹内脂肪含量与脂肪细胞因子、胰岛素抵抗的关系。方法分别检测36名肥胖2型糖尿病患者和20名正常体质量糖尿病患者的腹内脂肪含量、血清脂肪细胞因子(TNF-α、IL-6、瘦素、脂联素)水平及空腹血糖、空腹胰岛素等指标。结果与对照组相比,肥胖组的腹内脂肪含量Homa-IR、TNF-α、IL-6、瘦素显著升高,而脂联素显著降低(P0.05)。肥胖组患者的腹内脂肪含量与TNF-α、IL-6、瘦素水平正相关,与脂联素水平负相关(P0.05)。线性回归分析显示腹内脂肪含量是Homa-IR的独立影响因素。结论肥胖糖尿病患者腹内脂肪的积聚可加重胰岛素抵抗,其机制可能部分与腹内脂肪组织分泌的细胞因子有关。     

瘦素与肥胖 高血压的初步探讨

瘦素(leptin)是Zhang等[1]在1994年发现由肥胖基因编码,脂肪细胞合成分泌的肽类激素。它是一种脂肪组织分泌的脂源性内分泌多肽激素,进入血液循环后作用于瘦素受体,参与糖、脂肪及能量代谢的调节,促使机体减少摄食、增加能量释     

解偶联蛋白与肥胖及运动的关系

目的:解偶联蛋白(Uncouplingproteins,UCPS)可以驱散质子电化学梯度,使呼吸链和ATP的合成解偶联,从而影响产热和能量代谢。目前已发现5种UCPS家族成员,它们之间具有不同程度的同源性。UCPS现已被列为肥胖的候选基因。通过了解UCPS的作用机制、UCPS多态性与肥胖的关系及其表达的调节因素等,可以为肥胖发生机制及其防治工作的研究开辟新途径。资料来源:应用计算机检索1994/2004Medline的相关文章,检索词“Uncouplingproteins”,并限定文章语言种类为英文。同时计算机检索1994/2004中国期刊全文数据库(http://www.sy.cnki.net)的相关文章,限定文章语言种类为中文,检索项“关键词”,检索词“解偶联蛋白”,选择医药卫生辑专栏目录。另外手工检索到相关文献5篇。资料选择:对资料进行初审,被选文献符合以下标准:①解偶联蛋白家族中各成员研究。②解偶联蛋白与肥胖方面的研究。③解偶联蛋白与运动关系的研究。资料提炼:共收集到35篇相关文献,中文文献均为全文,部分外文文献为全文,其他为摘要。在这些文献中符合标准的有22篇。资料综合:UCP1在人体能量平衡中的作用不大。UCP2和UCP3与肥胖和2型糖尿病的发生可能有一定的相关性。UCP4基因表达于大鼠脂肪组织中,并可能参与肥胖的发生发展。摄食状况是影响UCPs基因表     

脂联素及其与运动的关系

目的:总结并分析脂联素研究进展,以及脂联素与运动的关系,为肥胖、代谢综合征、2型糖尿病、心血管疾病的治疗提供理论依据。资料来源:检索Medline1995-01/2006-10关于肥胖及运动减肥的文章。检索词"training,exercise,adiponectin,leptin"并限定文章的语种类为English。同时检索中国期刊全文数据库1994-01/2006-10关于肥胖及运动减肥的文章,限定文章语言种类为中文,检索词"运动,脂联素,瘦素"。资料选择:对资料进行初审,纳入标准:①关于脂联素的生理功能、信号转导及其与疾病的关系。②运动对脂联素的影响。排除标准:排除重复性研究。资料提炼:共收集到符合上述要求的文献213篇,对内容重复及与主题关系较远的文章进行筛除,32篇符合纳入标准。资料综合:脂联素和人的新陈代谢密切相关。主要影响脂联素的水平的因素有:脂联素复合体生物活性类型;年龄、性别、种族差异;瘦素、肿瘤坏死因子α、糖皮质激素、cAMP和β肾上腺素受体的激动剂、一氧化氮等因子的变化;其受体的活性。运动对脂联素影响方面的研究,结果有很大的不同,有人认为运动训练虽然能够改善糖尿病患者或代谢综合征的胰岛素抵抗,但并不能提高脂联素的水平;还有的研究者认为,运动训练改善胰岛素敏感性和运动训练改善了血浆中脂联素的浓度有关。结论:脂联素作为脂肪组织分泌的一种新的脂肪细胞因子,对于治疗肥胖、代谢综合征、2型糖尿病、心血管疾病具有重要的意义。目前国外对脂联素的生物功能,信号转导等进行了多方面的实验研究,而我国这方面的研究还较少。运动对脂联素的影响争议较多,需要严密对照设计的研究,以提示脂联素与运动的关系。     

Lipolysis and lipogenesis from glucose in human fat cells of different sizes: Effects of insulin, epinephrine, and theophylline

Lipogenesis from glucose and lipolysis in human omental and subcutaneous fat cells were studied as functions of adipose cell size and number in adult females. Since subcutaneous fat cells were larger than those prepared from the greater omentum, a comparison could be made of the metabolism of different sizes of cells within individual subjects. Rates per cell of glyceride-glycerol and glyceride-fatty acid synthesis from glucose were similar in omental and subcutaneous fat cells incubated in the presence or absence of insulin. However, subcutaneous fat cells exhibited higher rates of basal lipolysis than omental fat cells and these differences were maintained when lipolysis was stimulated with theophylline. Different rates of lipolysis were not demonstrable after incubations with epinephrine, indicating that subcutaneous fat cells were less responsive to this hormone than smaller omental fat cells. Correlation and partial correlation analysis showed that differences in basal and theophylline-stimulated lipolysis between fat cells prepared from different subjects and between omental and subcutaneous fat cells could be accounted for by differences in adipose cell volume. In subcutaneous fat cells highly significant intercorrelations were demonstrated between cell volume, basal lipolysis, and the basal conversion of glucose to glyceride-glycerol. There was no correlation between fat cell volume, age, or relative obesity and the effects of theophylline or insulin on lipolysis or lipogenesis from glucose in vitro when the data were expressed as percentage changes above basal values.     

Molecular mechanism in the development of the complications associated with obesity--the physiological and pathological role of adipocytokines

Visceral fat accumulation often accompanies various complications, such as insulin resistance, hypertension, dyslipidemia and atherosclerosis. Adipose tissue has been found to secrete various biologically active adipocytokines including free fatty acids. Accumulation of visceral fat increases the portal free fatty acids concentration to cause insulin resistance and dyslipidemia. Tumor necrosis alpha (TNF alpha) deteriorates insulin resistance in obesity. The levels of plasminogen activator inhibitor(PAI)-1 increase and plasma adiponectin concentration decreases in obesity leading to the development of vascular disease. The finding of genes specifically expressed in visceral fat and new adipocytokines should facilitate clarification of the mechanism for the development and complications of visceral fat accumulation.     

银杏叶提取物对老年性疾病的治疗作用

目的介绍近几年银杏叶提取物治疗老年病的概况,为其进一步的临床应用和科研设计提供参考资料.资料来源检索清华全文数据库1994-01/2005-10.关于银杏叶提取物和老年疾病、心脑血管相关的文章,限定文章语言种类为中文,检索词"银杏叶提取物,老年,心脑血管".资料选择对资料进行初审,选取包括处理组和对照组的文献,筛除明显不随机的研究,对剩余的文献开始查找全文.纳入标准为①随机对照研究.②实验或临床研究包含平行对照组.③处理组为应用银杏叶制剂.排除标准重复性研究.资料提炼共收集到221篇关于银杏叶提取物治疗老年性疾病的随机和未随机研究文章,25个动物实验或临床研究符合纳入标准.排除的196篇文章,175篇为未随机研究或重复性研究,2l篇为综述类文章.资料综合25个试验包括约1 099例患者和355只实验动物,证实了银杏叶提取物在糖尿病治疗方面具有调节血脂水平,从而改善胰岛抵抗作用;在高血压方面有效地改善老年高血压患者的高凝状态并改善血液流变性;在心脑血管方面能保护缺血性心肌,提高大鼠脑去甲肾上腺素、5-羟色胺含量,可通过上调Bcl-2蛋白表达,下调Bax蛋白表达,对脑缺血再灌注损伤起保护作用,能够明显改善脑梗死伴糖尿病患者的各项血液流变学特性;在抗衰老、老年痴呆方面能保护脑组织ATP酶的活性,抑制氧自由基对线粒体核糖核酸的损害而延缓老年大鼠脑衰老的进程,改善老龄大鼠的学习和记忆功能.银杏叶提取物已用于高血压、糖尿病、脑衰老、老年痴呆、心脑血管等疾病的治疗;无副性事件报道.结论银杏叶提取物是一种很有前途和价值的药物,在老年病的治疗领域中具有广阔的应用前景.     

Dysfunctional fat cells, lipotoxicity and type 2 diabetes

Type 2 diabetes is characterized by insulin resistance and impaired insulin secretion. Considerable evidence implicates altered fat topography and defects in adipocyte metabolism in the pathogenesis of type 2 diabetes. In individuals who develop type 2 diabetes, fat cells tend to be enlarged. Enlarged fat cells are resistant to the antilipolytic effects of insulin, leading to day-long elevated plasma free fatty acid (FFA) levels. Chronically increased plasma FFA stimulates gluconeogenesis, induces hepatic and muscle insulin resistance, and impairs insulin secretion in genetically predisposed individuals. These FFA-induced disturbances are referred to as lipotoxicity. Enlarged fat cells also have diminished capacity to store fat. When adipocyte storage capacity is exceeded, lipid 'overflows' into muscle and liver, and possibly the beta-cells of the pancreas, exacerbating insulin resistance and further impairing insulin secretion. In addition, dysfunctional fat cells produce excessive amounts of insulin resistance-inducing, inflammatory and atherosclerosis-provoking cytokines, and fail to secrete normal amounts of insulin-sensitizing cytokines. As more evidence emerges, there is a stronger case for targeting adipose tissue in the treatment of type 2 diabetes. Peroxisome-proliferator activated receptor gamma (PPARgamma) agonists, for example the thiazolidinediones, redistribute fat within the body (decrease visceral and hepatic fat; increase subcutaneous fat) and have been shown to enhance adipocyte insulin sensitivity, inhibit lipolysis, reduce plasma FFA and favourably influence the production of adipocytokines. This article examines in detail the role of adipose tissue in the pathogenesis of type 2 diabetes and highlights the potential of PPAR agonists to improve the management of patients with the condition.     

CDK4 is an essential insulin effector in adipocytes

Insulin resistance is a fundamental pathogenic factor that characterizes various metabolic disorders, including obesity and type 2 diabetes. Adipose tissue contributes to the development of obesity-related insulin resistance through increased release of fatty acids, altered adipokine secretion, and/or macrophage infiltration and cytokine release. Here, we aimed to analyze the participation of the cyclin-dependent kinase 4 (CDK4) in adipose tissue biology. We determined that white adipose tissue (WAT) from CDK4-deficient mice exhibits impaired lipogenesis and increased lipolysis. Conversely, lipolysis was decreased and lipogenesis was increased in mice expressing a mutant hyperactive form of CDK4 (CDK4^R24C). A global kinome analysis of CDK4-deficient mice following insulin stimulation revealed that insulin signaling is impaired in these animals. We determined that insulin activates the CCND3-CDK4 complex, which in turn phosphorylates insulin receptor substrate 2 (IRS2) at serine 388, thereby creating a positive feedback loop that maintains adipocyte insulin signaling. Furthermore, we found that CCND3 expression and IRS2 serine 388 phosphorylation are increased in human obese subjects. Together, our results demonstrate that CDK4 is a major regulator of insulin signaling in WAT.     

骨代谢与年龄增长的关系

目的:总结并分析随年龄增长人体骨代谢的特征,探讨随年龄增长骨骼的变化,重点探讨老年人,尤其闭经后妇女骨代谢的特征,为防治骨质疏松症提供科学依据。资料来源:应用计算机检索Medline1993-01/2003-12年龄增长与骨代谢文章。检索词为“Thebonemetabolism,Theagegrowth,”并限定文章语种为English。同时从图书馆人工检索1993-01/2003-12的日文资料中有关年龄增长与骨代谢相关的文章。资料选择:对资料进行初审,纳入标准:①关于随年龄增长骨骼的生理性变化特征、机制、影响因素。②对临床病例回顾性研究分析;排除重复性研究内容。资料提练:符合上述要求的文章21篇,排除14篇重复性研究。7篇符合纳入标准:其中3篇为研究性论著,2篇为诊断标准,2篇为教科书。资料综合:随年龄增长骨代谢变化很大,在生长期骨骼逐渐成熟,骨骼钙量逐渐增加。一般到20岁以后骨代谢处于动态平衡,40岁以后骨代谢呈负增长,骨骼钙量减少。骨代谢变化是随年龄增长最剧烈、变化量最大的一个参数。老年人,尤其是妇女闭经后骨质疏松发生率增长很快,除因老年人退行性变外,还与内分泌紊乱等多种因素相关,通过研究为防治骨质疏松症提供科学依据。结论:在了解年龄增长与骨代谢关系的基础上,认识到防治骨质疏是可能的,主要是建立健康的生活方式,注意营养全面,摄入足量的含钙高的食物。     

Insulin resistance

Insulin resistance is closely associated with fat accumulation in liver. Thus, it has been suggested that insulin resistance is one of the important factor in development of non-alcoholic steatohepatitis(NASH). For example, insulin resistance in adipocyte results in increased lipolysis and delivery of free fatty acids(FFAs) to the liver, which induce fatty liver. If there is insulin resistance in skeletal muscle, hyperinsulinemia and/or hyperglycemia might increase fat accumulation in liver, through, at least in part, increased sterol-regulatory element binding protein-1c(SREBP-1c) activation. However, hepatic insulin resistance might prevent fat accumulation in liver, because insulin strongly induces lipogenesis. Thus, the tissue specific insulin resistance should be considered in the pathogenesis of NASH.     

Interplay between FGF21 and insulin action in the liver regulates metabolism

The hormone FGF21 regulates carbohydrate and lipid homeostasis as well as body weight, and increasing FGF21 improves metabolic abnormalities associated with obesity and diabetes. FGF21 is thought to act on its target tissues, including liver and adipose tissue, to improve insulin sensitivity and reduce adiposity. Here, we used mice with selective hepatic inactivation of the IR (LIRKO) to determine whether insulin sensitization in liver mediates FGF21 metabolic actions. Remarkably, hyperglycemia was completely normalized following FGF21 treatment in LIRKO mice, even though FGF21 did not reduce gluconeogenesis in these animals. Improvements in blood sugar were due in part to increased glucose uptake in brown fat, browning of white fat, and overall increased energy expenditure. These effects were preserved even after removal of the main interscapular brown fat pad. In contrast to its retained effects on reducing glucose levels, the effects of FGF21 on reducing circulating cholesterol and hepatic triglycerides and regulating the expression of key genes involved in cholesterol and lipid metabolism in liver were disrupted in LIRKO mice. Thus, FGF21 corrects hyperglycemia in diabetic mice independently of insulin action in the liver by increasing energy metabolism via activation of brown fat and browning of white fat, but intact liver insulin action is required for FGF21 to control hepatic lipid metabolism.     

The Influence of Body Weight and Cell Size on Lipogenesis and Lipolysis of Isolated Rat Fat Cells*

Abstract. A method for fractionating isolated fat cells is described. After fixation with osmium tetroxide, the cells are passed through a series of polyamide filters of decreasing mesh width and the number of cells on each filter is counted. – Isolated fat cells from ad libitum fed rats weighing 85–580 g were incubated with [U-¹⁴C]-glucose (0.55 mM), fixed with osmium tetroxide and fractionated according to size. When the cells were obtained from one animal the conversion of glucose to neutral lipids per cell increased with increasing cell size just as well in the absence of insulin as in the presence of insulin (10 mU/ml). The following results were obtained from comparisons between animals of different weight: in the absence of insulin, the lipogenesis for cells of the same size remained constant irrespective of the rat weight, whereas in the presence of insulin the lipogenesis for cells of the same size decreased markedly when the rat weight exceeded about 300 g. It is concluded that factors other than the cell size per st (e.g. age, degree of obesity) determine the responsiveness to insulin. – The hormone-stimulated lipolysis was studied on unfractionated cell samples from ad libitum fed rats of different weights and the following was found: the glycerol release per 10⁵ cells induced by ACTH and norepinephrine in maximally stimulating concentrations increased with increasing mean cell size or rat weight. In contrast, the glucagon-induced lipolysis of cells from rats weighing 300–400 g was smaller than that of cells from rats weighing 100–120 g.     

The influence of body weight and cell size on lipogenesis and lipolysis of isolated rat fat cells

Abstract. A method for fractionating isolated fat cells is described. After fixation with osmium tetroxide, the cells are passed through a series of polyamide filters of decreasing mesh width and the number of cells on each filter is counted. — Isolated fat cells from ad libitum fed rats weighing 85–580 g were incubated with [U-¹⁴ C]-glucose (0.55 mM), fixed with osmium tetroxide and fractionated according to size. When the cells were obtained from one animal the conversion of glucose to neutral lipids per cell increased with increasing cell size just as well in the absence of insulin as in the presence of insulin (10 mU/ml). The following results were obtained from comparisons between animals of different weight: in the absence of insulin, the lipogenesis for cells of the same size remained constant irrespective of the rat weight, whereas in the presence of insulin the lipogenesis for cells of the same size decreased markedly when the rat weight exceeded about 300 g. It is Concluded that factors other than the cell size per se (e.g. age, degree of obesity) determine the responsiveness to insulin. — The hormone-stimulated lipolysis was studied on unfractionated cell samples from ad libitum fed rats of different weights and the following was found: the glycerol release per 10⁶ cells induced by ACTH and norepinephrine in maximally stimulating concentrations increased with increasing mean cell size or rat weight. In contrast, the glucagon-induced lipolysis of cells from rats weighing 300–400 g was smaller than that of cells from rats weighing 100–120 g.